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Heart Failure/Angina

Drugs for HF and Angina

DrugIndicationPharmacokineticsAdverse EffectsNotesDrug Interactions
ACE Inhibitors Considered cornerstone of HF therapy. Block production of angII, dec. release of aldosterone, suppress degradation of kinins (ARBs don't do this). SO they improve hemodynamics and favorably alter cardiac remodeling hemodynamic benefits: arteriolar dilation improves regional blood flow in kidneys,promoting excretion of Na and H2O; Reducing afterload increases CO and SV;Venous dilation reduces venous pressure_>red. pulmonary congestion, periph. edema, preload and card Hypotension 2/2 arteriolar dilation; cough (bradykinin acc. 2/2 inhibition of ACE); angioedema; hyperkalemia 2/2 dec. aldosterone release; fetal injury; renal failure with low GFR in absence of contraindications, all HF should get ACEI
ARB improve LV ejection fraction, reduce HF symptoms, increase exercise tolerance, decrease hosp, enhance QOL, reduce mortality hypotension, angioedema, renal failure, fetal harm *do not increase levels of kinins, like AECI do, so effects on cardiac remodeling less favorable; so use for HF pts who cant tolerate ACEI (d/t cough)
Aldosterone Antagonists (eplerenone, spironolactone) reduce s/s, decrease hosp, prolong life in pts w/HF primary is hyperkalemia (risk increased by renal impairment and ACE/ARB use) measure baseline and monitor use if pts have severe symptoms
B Blockers (HF) can improve LV ejection fraction, increase exercise tolerance, slow progression of HF, reduce hosp, prolong survival fluid retention, worsening of HF, fatigue, hypotn, bradycardia or heart block (d/t reduction in contractility) since blockade of cardiac B1 receptors reduces contractility, doses must be low initially and increased gradually,and used w/ care
Digoxin (only cardiac glycoside approved in US) HF and control of dysrhythmias: +inotropic agent, increasing CO, MOA:inhibits Na-K-ATPase,promoting Ca accumulation w/in myocytes, augmenting contractile force absorption can vary w/ pharm company; crosses placenta;elim. primarily renally, so alterations in renal fxn can have profound impact on dig levels low K->digoxin toxicity, high K->low therapeutic response (s/s of toxicity: altered HR or rhythm, GI or visual disturbances) (when used for HF, can reduce s/s, increase exercise tolerance, and decrease hosp., but the drug does not prolong life,so consid. 2nd line agent) Therapeutic drug levels for HF:0.5-0.8 ng/ml, toxic>2ng/ml (narrow index) diuretics (hypokelmia->toxicity); ACEI/ARBs (hyperkalemia->dec. dig effects); sympathomimetics (additive inotropic effect);Amiodarone (dog tox due to inhibiton of p-glycoprotein); St. John's Wort; Quinidine; Verapimil
Sodium Nitroprusside (nitropress) short term therapy of severe refractory HF profound hypotn, so monitor BP continuously acts rapidly to dilate arterioles and veins; A dilation reduces afterload, increasing CO; V dilation reduces venous pressure, decreasing pulmonary and peripheral congestion
Nitrates (NTG, isosorbide mononitrate, isosorbide dinitrate) Act directly on vascular smooth muscle to promote vasodilation; stable angina: NTG dec. pain by decreasing cardiac O2 demand, by dilating veins, NTG dec. venous return to heart dec vent. filling, decrease in preload, decreases demand; Variant Angina: goal absorption:highly lipid soluble and crosses membranes w/ease;metabolism:nitrates undergo rapid inactivation by hepatic enzymes;tolerance:excessive use,esp. w/high dose and uninterrupted therapy.SO, use lowest effective dose, and using long-acting formulat headache, ortho hypotn, reflex tachy long acting preparations should be d/c slowly to prevent vasospasms
B Blockers (angina) reduce cardiac O2 demand by blockade of B1 receptors, decreasing HR and contractility; modest reductions in afterload, and slowing HR, increases time in diastole, can help increase O2 supply effects on CNS: depression, bizarre dreams, insomnia, sexual dysfunction, mask signs of hypoglycemia In pts taking vasodilators, BB can provide the additional benefit of blunting reflex tachy;should not be withdrawn abruptly,can increase angina intensity and even precipitate MI; NOT effective against Var.angina&should not be used in pts w/decompensated H
CCB (verapamil, diltiazem, nifedipine-dihydropyridine) arteriolar dilation and reduction of afterload; relax coronary vasospasm; D&V can block CC in heart induce reflex tachy (nifedipine); V&D are cardiosuppressors, so use cautiously in pts with BB, bradycardia, HF or AV block used for both var (increase o2 supply->relax coronary artery vasospasm) and stable angina (decrease O2 demand->decrease afterload)
Ranolazine treatment of chronic angina MOA not understood, but inhibits late Na current, reducing Na-induced Ca overload in myocytes prolongs QT interval, may increase risk of arrythmias; dizziness, constipation, headache, nausea NOT first line treatment metabolized through CYP3A4 inhibitors, and is a substrate for P-glycoprotein, veramipil and diltiezam should not be co-administered, since can lead to ranolazine toxicity
Diuretics First line therapy for pts with signs of FVE: decrease VP,AP(afterload),Pulmonary and peripheral edema,and cardiac dilation Do not overdiurese pt ->FVD, rx according to level of edema
Thiazides 1.don't diurese as much as loops 2. used for LT therapy of HF when edema is not too great 3. cannot be used if CO too low (GFR low) 4.principal adverse effect is hypokalemia (increasing risk of digoxin-induced dysrh)
Loop/High Ceiling Diuretics (furosemide) 1. produce profound diureses 2. can be used if GFR is low 3.preferred if HF is severe 4.can also cause hypokalemia (digoxin-induced dysrh) 5.severe hypotn 2/2 excessive volume reduction
K Sparing Diuretics 1. used primarily to maintain K levels 2.produce scant diuresis use caution when combined with ACE/ARBs
Created by: jellyfishh